Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “RESPIRATORY DISTRESS SYNDROME”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 505 records · Page 28Linked to original sources
PubMed1989

Adult respiratory distress syndrome from overdose of tricyclic antidepressants.

Adult respiratory distress syndrome (ARDS) from overdose of tricyclic antidepressants (TCA) has been reported but is not well known. During a 1-year period, 81 patients with serious overdose from tranquilizers and other psychotropic drugs were examined. TCA alone induced overdose in 30 patients or were combined with other drugs in 26 patients. Twenty-five (31%) patients had overdose from drugs other than TCA. Chest radiography revealed that 30 (54%) patients with TCA overdose and six (24%) patients with non-TCA overdose had abnormalities. Clinical and radiographic findings consistent with ARDS were noted in five (9%) patients with TCA overdose and none of the patients with non-TCA overdose. Five patients with TCA overdose and one (4%) patient with non-TCA overdose had interstitial edema that never progressed to ARDS. TCA should be added to the list of drugs associated with the development of ARDS.

Antidepressive Agents, Tricyclic↗
PubMed1994

[Natural and synthetic surfactant in the treatment of neonatal respiratory distress syndrome].

The results of treatment of severe respiratory distress syndrome in premature infants with gestational age < or = 32 weeks are reported. During the two-year period 1991-92, the department participated in both the Osiris study (Exosurf) and the Curosurf 4 study (Curosurf). Five of the 23 infants treated with Exosurf died and 16 survived without major sequelae. 14 of the 25 infants treated with Curosurf died and six survived without major sequelae. Four of the infants treated with Curosurf developed severe retinopathy of prematurity. During the study period this complication occurred in one additional patient who was not eligible for inclusion in the study. The results show the need to study differences in the physiological effects of surfactants more closely, in order both to improve the basis for selection of surfactant for individual patients, and to define the indications for treatment. The results raise the question of whether such studies should continue to include control patients.

Biological Products↗
PubMed1991

[Non-respiratory therapy of adult respiratory distress syndrome].

Several approaches to non-respiratory management of adult respiratory distress syndrome (ARDS) are discussed. (1) Diagnosis and therapy of the underlying disease is a primary goal in order to avoid the ongoing process of lung injury. (2) Specific pharmacologic therapy for primary lung injury is not available even after 25 years of immunologic research, because no specific mediator has yet been identified as a primary pathogenic factor in ARDS, which is a heterogenous clinical syndrome. (3) Supportive therapy (i.e. improving right ventricular dysfunction and treating pulmonary arterial hypertension) should be emphasized. (4) The most important approach is to optimize prophylactic management to avoid nosocomial infection by eliminating unnecessary invasive techniques, changing the patients' positioning and conserving organ function. So far the latter approach seems to be the only way to improve survival in respiratory failure.

Anti-Inflammatory Agents↗
PubMed2000

An approach to ventilation in acute respiratory distress syndrome.

Appropriate management of patients with acute respiratory distress syndrome (ARDS) represents a challenge for physicians working in the critical care environment. Significant advances have been made in understanding the pathophysiology of ARDS. There is also an increasing appreciation of the role of ventilator-induced lung injury (VILI). VILI is most likely related to several different aspects of ventilator management: barotrauma due to high peak airway pressures, lung overdistension or volutrauma due to high transpulmonary pressures, alveolar membrane damage due to insufficient positive end expiratory pressure levels and oxygen-related cell toxicity. Various lung protective strategies have been suggested to minimize the damage caused by conventional modes of ventilation. These include the use of pressure- and volume-limited ventilation, the use of the prone position in the management of ARDS, and extracorporeal methods of oxygen delivery and carbon dioxide removal. Although the death rate resulting from ARDS has been declining over the past 10 years, there is no evidence that any specific treatment or change in approach to ventilation is the cause of this improved survival.

Barotrauma↗
PubMed2004

[A case of acute respiratory distress syndrome (ARDS) caused by splenic infarction].

Acute respiratory distress syndrome (ARDS) is the most severe lung injury caused by many pathologic states. We treated a patient who suffered from ARDS caused by splenic infarction. A 75-year-old patient had a gastric cancer with multiple lung and liver metastasis. During anti-cancer therapy, she developed a high fever (above 39 degrees C) and a chest and an abdominal CT scan revealed splenic infarction. Hypoxia progressed gradually and she was transferred to ICU with tracheal intubation. Mechanical ventilation was performed according to open lung strategy, but she did not recover. On ICU day 3, the bilateral infiltration shadow on her chest X-ray was pointed out, and she had a low central venous pressure. We diagnosed her ARDS. The administration of methylprednisolone was started according to Meduri's report. Hypoxia was improved gradually and on ICU day 7, she was weaned from mechanical ventilation, and extubated. On ICU day 8, she was returned to her ward without ventilatory support.

Aged↗
PubMed1983

[Reduction of pulmonary capillary volume following acute respiratory distress syndrome in adults].

Lung function after adult respiratory distress syndrome was evaluated in 8 survivors whose ages ranged from 20 to 54 years. At the time of the study, 5.5 to 19 months after extubation, all patients were asymptomatic at rest but 6 had mild to moderate exertional dyspnea. Physical examination was normal in 7 patients; lung volumes, flow rates and pulmonary mechanics were minimally altered, mainly in smokers. Chest X-rays showed no major abnormalities. On graded submaximal exercise test, performance was limited by tachycardia and not by ventilation. Resting arterial PO2 was low in 6 patients and increased only in one patient during submaximal exercise. The capillary blood volume was decreased in all patients. The mechanisms of hypoxia during exercise and decreased capillary blood volume, the latter apparently unrelated either to pulmonary microvascular obstruction or to fibrosis, remain unexplained. It is concluded that lung volumes and pulmonary mechanics are restored to normal within 6 months after ARDS, whereas gas exchanges persist after ARDS and are associated with a reduced pulmonary blood volume.

Acute Disease↗
PubMed1994

CT and chest radiography in the evaluation of adult respiratory distress syndrome.

CT is seldom employed in adult respiratory distress syndrome (ARDS), mostly due to problems in transporting and monitoring these severely ill patients. We reviewed the findings of 74 ARDS patients who underwent chest CT. Lung opacities were bilateral in almost all patients and dependent in most cases (86%). The opacities were patchy (42%), homogeneous (23%), ground glass (8%) or mixed (27%). Opacities prevailed in basal regions (68%) compared to hilar and apical ones. Air bronchograms were frequently seen in areas of consolidation (89%). In contrast with previous reports, pleural effusion was a frequent finding (50%) that did not worsen prognosis. Often loculated pneumothorax (32%) was mostly anteromedial. Ineffective position of thoracostomy tubes was detected at CT in 13/20 patients. Pulmonary air cysts (30%), always multiple and mostly bilateral, were associated with a higher mortality (55%) than that of the whole study group (35%). Compared to chest radiographs, CT often yielded additional information (66%), with direct influence on patient treatment in 22% of cases.

Adolescent↗
PubMed1992

Ketoconazole inhibits alveolar macrophage production of inflammatory mediators involved in acute lung injury (adult respiratory distress syndrome).

BACKGROUND: Acute inflammatory lung injury (adult respiratory distress syndrome [ARDS]) causes significant morbidity and death in surgical patients. The alveolar macrophage elaborates proinflammatory mediators implicated in acute pulmonary injury. The macrophage products, leukotriene B4 (LTB4), thromboxane A2 (TXA2), and procoagulant activity (PCA), initiate inflammatory cascades that lead to microvascular thrombosis and neutrophil infiltration, two common features of ARDS. One potential method of preventing or attenuating lung injury is to inhibit the production of inflammatory mediators. Preliminary studies indicate that ketoconazole, known primarily for its antifungal properties, may prevent ARDS. METHODS: LTB4, TXB2, and PCA production by rabbit alveolar macrophages was measured after treatment with endotoxin or Ca ionophore and ketoconazole or selective 5-lipoxygenase (MK 886) and thromboxane synthetase (imidazole) inhibitors. RESULTS: Ketoconazole significantly inhibits alveolar macrophage production of LTB4, TXB2, and PCA. Ketoconazole inhibition of PCA is independent of effects on 5-lipoxygenase and thromboxane synthetase. CONCLUSIONS: Ketoconazole inhibition of alveolar macrophage proinflammatory mediators may be of benefit in preventing ARDS by minimizing neutrophil infiltration and microvascular thrombosis. Inhibition of 5-lipoxygenase and thromboxane synthetase, without affecting cyclooxygenase, may offer a selective advantage by allowing production of other homeostatic eicosanoids.

Animals↗
PubMedDate not supplied

Distinguishing between infection, rejection, and the adult respiratory distress syndrome after human lung transplantation.

The adult respiratory distress syndrome, bacterial pneumonia, cytomegalovirus pneumonitis, acute rejection, or a combination thereof were the primary causes of radiographic infiltrates or gas exchange abnormalities that occurred early after lung transplantation. The time of occurrence after transplantation, standard measures of clinical assessment as for nontransplant patients (i.e., vital signs, weight, white blood cell count, sputum, and cultures, etc.), bronchoalveolar lavage, and transbronchial lung biopsy were the primary tools used to analyze these situations. Bacterial pneumonia always occurred after postoperative day 2, acute rejection after postoperative day 5, and cytomegalovirus pneumonitis after postoperative day 16. Although cultures of bronchoalveolar lavage fluid were useful to detect pneumonia caused by bacteria, virus, and fungus, the types of cells recovered by bronchoalveolar lavage were not diagnostic of any type of disorder. Transbronchial lung biopsy was necessary to detect acute rejection and cytomegalovirus pneumonitis. Thus the cause of an early radiographic infiltrate or impairment of gas exchange was almost always reliably determined by using standard tools of clinical assessment, knowledge of the usual temporal sequence of the complications, and judicious use of bronchoalveolar lavage and transbronchial lung biopsy.

Biopsy↗
PubMed2000

Tracheal gas insufflation. Limits of efficacy in adults with acute respiratory distress syndrome.

In mechanically ventilated adults with acute respiratory distress syndrome (ARDS), peak airway pressures (Paw(peak)) above 35 cm H(2)O may increase the risk of barotrauma or volutrauma. Tracheal gas insufflation (TGI), an adjunctive ventilatory technique, may facilitate a reduction in set inspiratory pressure in these patients, and thereby in the tidal volume (VT) and Paw(peak) used in their ventilation, without a consequent increase in arterial carbon dioxide tension (PaCO(2)). The purpose of this study was to: (1) assess the limits of efficacy of continuous TGI at two levels of decreased mechanical ventilatory support; and (2) determine an appropriate time interval after initiation of TGI at which to evaluate response. We prospectively studied eight adults with ARDS and increased airway pressures (40.2 +/- 2.7 cm H(2)O) who were managed with pressure-control ventilation (PCV). After obtaining baseline ventilatory and hemodynamic measures, we initiated TGI at 10 L/min, adjusting ventilator positive-end expiratory pressure (PEEP) to maintain baseline VT, and decreased the set inspiratory pressure by 5 cm H(2)O. Data were obtained after 30 and 60 min. Set inspiratory pressure was then decreased by an additional 5 cm H(2)O (total: 10 cm H(2)O), and data were again obtained after 30 min. Baseline (zero TGI) measures were then again recorded. Thirty minutes after decreasing the set inspiratory pressure by 5 cm H(2)O with TGI at 10 L/min, there was a 15% decrease in Paw(peak) and a 16% decrease in VT as compared with their baseline values. However, Pa(CO(2)) remained constant (59 +/- 10 mm Hg versus 57 +/- 6 mm Hg) (p = NS). There was no change in Pa(O(2)) or in hemodynamic variables, and no differences between variables, at 30 min versus 60 min in seven subjects. The remaining subject did not tolerate the reduction in set inspiratory pressure for 60 min. Thirty minutes after the set inspiratory pressure was decreased by 10 cm H(2)O with TGI at 10 L/min, there was a 26% decrease in Paw(peak) and a 26% decrease in VT. However, Pa(CO(2)) increased by 19% and Pa(O(2)) decreased by 13%. Six subjects completed this phase of the protocol for 30 min, and one subject completed it for 60 min. TGI can be used to rapidly facilitate a 5 cm H(2)O reduction in set inspiratory pressure without an increase in Pa(CO(2)). The ability to achieve a 5 cm H(2)O reduction in set inspiratory pressure without adverse physiologic effects was evident within 30 min. Attempts to further reduce set inspiratory pressure were not successful.

Acute Disease↗
PubMed1991

Cost implications of different approaches to the prevention of respiratory distress syndrome.

Because the incidence of both neonatal respiratory distress syndrome and neonatal mortality can be reduced by giving corticosteroids to women expected to deliver preterm and by giving surfactant to babies at high risk of developing hyaline membrane disease, we have considered what effects the adoption of one or both of these preventive policies would have on the costs of neonatal care. We have estimated the effects of treatment from overviews of the relevant controlled trials, and estimated costs from observations of care at one neonatal unit. Our results suggest that if either of these policies is adopted for all babies under 35 weeks' gestation at a drug cost of 150 pounds or less/baby, the overall costs of care would be reduced by between 1 and 10%. The cost per survivor would be reduced by up to 16% even if the drug cost were to be as high as pounds 550/baby. If the policies were to be adopted only for babies under 31 weeks' gestation, both policies would result in a reduction in cost of between 5 and 16%/survivor, although the increased survival resulting from the policies would lead to an increase in overall costs for babies of less then 31 weeks' gestation of between 7 and 32%.

Adrenal Cortex Hormones↗
PubMed2006

Mechanical ventilation and air leaks after lung biopsy for acute respiratory distress syndrome.

BACKGROUND: Open lung biopsy in acute respiratory distress syndrome (ARDS) may provide a specific etiology and change clinical management, yet concerns about complications remain. Persistent air leak is the most common postoperative complication. Risk factors in this setting are not known. METHODS: We performed a retrospective analysis of 53 patients who underwent open lung biopsy for clinical ARDS (based on American European Consensus Conference criteria) between 1989 and 2000. RESULTS: Sixteen patients (30.2%) developed an air leak lasting more than 7 days or died with an air leak. Univariate analyses showed no significant correlation with age, gender, sex, corticosteroid use, diabetes, immunocompromised status, or pathologic diagnosis. A lower risk of air leak was associated with lower peak airway pressure and tidal volume, use of pressure-cycled ventilation, and use of an endoscopic stapling device. In multivariate analyses, only peak airway pressure remained a significant predictor. The risk of prolonged air leak was reduced by 42% (95% confidence interval [CI: 17% to 60%]) for every 5 cm H2O reduction in peak airway pressure. CONCLUSIONS: The use of a lung-protective ventilatory strategy that limits peak airway pressures is strongly associated with a reduced risk of postoperative air leak after open lung biopsy in ARDS. Using such a strategy may allow physicians to obtain information from open lung biopsy to make therapeutic decisions without undue harm to ARDS patients.

Adult↗
PubMed1989

Prostaglandin E1 and nitroglycerin reduce pulmonary capillary pressure but worsen ventilation-perfusion distributions in patients with adult respiratory distress syndrome.

Pulmonary artery hypertension associated with adult respiratory distress syndrome (ARDS) may increase microvascular filtration pressure by increasing pulmonary capillary pressure (PCP). To evaluate the potential to reverse this consequence of pulmonary artery hypertension, the effects of short-term vasodilator treatment were compared with prostaglandin E1 (PGE1) or nitroglycerin (NTG) on pulmonary hemodynamics and gas exchange. The two vasodilators were infused in ten patients with mild or moderate ARDS at a dosage rate achieving a 20% reduction of the mean arterial pressure. PCP was estimated by graphic analysis of the pulmonary artery occlusion curve, and continuous ventilation-perfusion (VA/Q) distributions were assessed using the multiple inert gas technique. At the given dosages both drugs induced equivalent reductions of the mean pulmonary artery pressure (PAP) from 28.2 +/- 3.6 to 23.7 +/- 3.2 with PGE1 and to 23.4 +/- 3.2 mmHg with NTG. The right atrial and pulmonary artery wedge pressure (PAWP) were also decreased to the same extent associated with the expected decrease in PCP from 17.4 +/- 2.6 to 15.1 +/- 3.3 with PGE1 and to 15.6 +/- 2.7 mmHg with NTG. The estimated PCP values were closely correlated with the values calculated according to Gaar's equation (r = 0.822. n = 23, P less than 0.001) with a regression close to the identity line. The contribution of pulmonary venous resistances to the resistance of the whole pulmonary vascular bed computed as the ratio (PCP- PAWP)/(PAP-PAWP) was 0.28 and remained unchanged during vasodilator infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

[Albumin and fibronectin dynamics in an experimental adult respiratory distress syndrome model].

We produced an experimental adult respiratory distress syndrome model by intravenous administration of oleic acid (OA) in 30 dogs (Group I: 10 normal dogs; Group II: 10 dogs with 0.02 ml/kg of OA; Group III: 10 dogs with 0.04 ml/kg of OA; Group IV: 10 dogs with 0.08 ml/kg of OA). Changes in albumin (AL) and fibronectin (FN) in serum and BALF of these dogs were examined. The following results were obtained: 1) Serum values of AL and FN were significantly decreased after OA injection as compared with the baseline values. These changes were not correlated with the severity of pulmonary edema. 2) BALF values of AL and FN were significantly increased after OA injection as compared with the baseline values. Significant linear correlations were found between the BALF value of AL and ELWV, and between BALF value of AL and delta ELWV, [r = -0.682, 0.573 (p < 0.01)]. Significant linear correlations were also found between the BALF value of FN and ELWV, and the BALF value of FN and delta ELWV, [r = 0.722, 0.650 (p < 0.01)]. BALF value of AL increased significantly even with the low OA dose (0.02 ml/kg). Thus in comparison with BALF value of AL after OA injection, BALF value of FN was significantly higher than that in the normal group even when pulmonary edema were severe (Groups III and IV). We concluded that we could estimate the severity of pulmonary edema by measuring BALF value of AL and FN simultaneously.

Animals↗
PubMed1994

Influence of positioning on ventilation-perfusion relationships in severe adult respiratory distress syndrome.

In 12 patients with severe adult respiratory distress syndrome (ARDS), pulmonary gas exchange and hemodynamics were evaluated before, during, and after a 2-h period of pressure-controlled mechanical ventilation with the patient in the prone position. Ventilation-perfusion relationships (VA/Q) were assessed by a multiple inert gas elimination technique. Pressure-controlled mechanical ventilation in the prone position resulted in an overall increase (p < or = 0.05) of arterial oxygenation after 120 min (98.4 +/- 50.3 to 146.2 +/- 94.9 mm Hg). Whereas eight patients revealed an improvement of PaO2 of more than 10 mm Hg after 30 min in the prone position (responders), four patients reacted to positional changes with a deterioration of arterial oxygenation (nonresponders). Data about the continuous distribution of ventilation-perfusion ratios revealed that in the responder group positioning caused a decrease of shunt perfusion of 11 +/- 5% and a concomitant increase of normal VA/Q by 12 +/- 4% after 30 min. There was no change demonstrable within low VA/Q areas. Returning the patient to the supine position reversed the improvement in gas exchange. The nonresponder group did not show any significant alteration in the distribution of VA/Q during the study. We concluded that improvement of oxygenation during pressure-controlled mechanical ventilation in the prone position is due to a shift of blood flow away from shunt regions, thus increasing areas with normal VA/Q. This redistribution of blood flow is most likely caused by a recruitment of previously ateletatic but nondiseased areas induced by altered gravitational forces.

Adolescent↗
PubMed2001

Surfactant treatment in premature infants with Respiratory Distress Syndrome in Curaçao.

Surfactant replacement therapy for Respiratory Distress Syndrome (RDS) in premature neonates has been established as an effective treatment, although significant mortality and morbidity remain. In Curaçao, surfactant became available as a therapeutic option in 1994. A retrospective cohort study was performed to describe the results of surfactant treatment in premature newborns with RDS in Curaçao between 1994 and 1998. Of 429 infants admitted to the study hospital in this period, 7.5% (n = 32) developed RDS and were treated with surfactant. Twenty-five per cent (n = 8) of these infants died, most of them in the first year of surfactant treatment. Twenty-eight per cent (n = 9) developed bronchopulmonary dysplasia (BPD), the most frequently observed complication. The highest incidence of BPD (44%) was found in the very low birth weight infants (750-1500 g); all infants with BPD were 27-30 weeks of gestational age. The duration of ventilator dependence was significantly associated with the development of BPD (p < 0.05). No other risk factors for complications during the treatment course could be identified. The mean time between birth and the first surfactant treatment was more than nine hours. In this study, we found low incidence rates of RDS and BPD, and a considerable mortality in surfactant treated newborns. This pilot study shows that surfactant treatment of premature infants is feasible in Curaçao. Earlier administration of surfactant, preferably within 2-3 hours after birth, is expected to lower the risk of death and oxygen dependence.

Bronchopulmonary Dysplasia↗
PubMed2005

Pathophysiology of neonatal respiratory distress syndrome: implications for early treatment strategies.

Neonatal respiratory distress syndrome (RDS) remains one of the major causes of neonatal mortality and morbidity despite advances in perinatal care. The initial management of infants with RDS has almost become 'too routine' with little thought about the pathophysiological processes that lead to the disease and how the clinician can use the existing therapeutic interventions to optimize care. The transition from fetus to infant involves many complex adaptations at birth; the most important is the function of the lungs as a gas exchange organ. Preterm surfactant-deficient infants are less well equipped to deal with this transition. Optimum gas exchange is achieved through matching of ventilation and perfusion. In RDS, ventilation may be affected by homogeneity of the airways with atelectasis and over distension, as hyaline membranes block small airways. In turn this contributes to the inflammation that becomes bronchopulmonary dysplasia. Exogenous surfactant given early, particularly with positive end-expiratory pressure and, where necessary, gentle ventilation, would seem to be the optimum way to prevent atelectasis. How this can be achieved in neonates after surfactant therapy is explored through a review of the normal physiology of the newborn lung and how this is affected by RDS. The therapeutic interventions of resuscitation, exogenous surfactant, ventilation and inhaled nitric oxide are discussed in relation to their effects and what are currently the optimum ways to use these. It is hoped that with a better understanding of the normal physiology in the newborn lung, and the effects of both disease and interventions on that physiology, the practising clinician will have a greater appreciation of management of preterm infants with, or at risk of, RDS.

Humans↗
PubMed1998

Inhaled nitric oxide for adult respiratory distress syndrome after pulmonary resection.

BACKGROUND: The adult respiratory distress syndrome (ARDS) developing after pulmonary resection is usually a lethal complication. The etiology of this serious complication remains unknown despite many theories. Intubation, aspiration bronchoscopy, antibiotics, and diuresis have been the mainstays of treatment. Mortality rates from ARDS after pneumonectomy have been reported as high as 90% to 100%. METHODS: In 1991, nitric oxide became clinically available. We instituted an aggressive program to treat patients with ARDS after pulmonary resection. Patients were intubated and treated with standard supportive measures plus inhaled nitric oxide at 10 to 20 parts/million. While being ventilated, all patients had postural changes to improve ventilation/perfusion matching and management of secretions. Systemic steroids were given to half of the patients. RESULTS: Ten consecutive patients after pulmonary resection with severe ARDS (ARDS score = 3.1+/-0.04) were treated. The mean ratio of partial pressure of arterial oxygen to the fraction of inspired oxygen at initiation of treatment was 95+/-13 mm Hg (mean +/- SEM) and improved immediately to 128+/-24 mm Hg, a 31%+/-8% improvement (p<0.05). The ratio improved steadily over the ensuing 96 hours. Chest x-rays improved in all patients and normalized in 8. No adverse reactions to nitric oxide were observed. CONCLUSIONS: We recommend the following treatment regimen for this lethal complication: intubation at the first radiographic sign of ARDS; immediate institution of inhaled nitric oxide (10 to 20 parts per million); aspiration bronchoscopy and postural changes to improve management of secretions and ventilation/perfusion matching; diuresis and antibiotics; and consideration of the addition of intravenous steroid therapy.

Administration, Inhalation↗